Genotype of FLOWERING LOCUS T homologue contributes to flowering time differences in wild and cultivated roses

Rose flowers have long delighted humans as ornamental plants. To improve the ornamental value of roses it is necessary to understand the regulatory mechanisms of flowering. We previously found that flowering time is controlled by three minor quantitative trait loci (QTLs) and a major QTL co-localised with RoFT. In this study, we isolated three RoFT alleles encoding completely identical amino acid sequences from the parents of a mapping population. Correlation analysis of the RoFT genotypes and flowering time phenotypes in the mapping population showed that the RoFT_f and RoFT_g alleles contribute to the early-flowering phenotype, while the RoFT_e allele contributes to the late-flowering phenotype. We developed two novel cleaved amplified polymorphic sequence (CAPS) markers based on the genomic sequences of the RoFT alleles and clearly showed that the relationship between RoFT genotype and flowering time was applicable to 12 of 13 cultivated roses grown at the Higashiyama Botanical Gardens, Japan. Allele-specific expression analysis using a reverse transcription CAPS assay suggested that these RoFT alleles are regulated differentially at the transcription level. Furthermore, transgenic Arabidopsis thaliana plants ectopically expressing the RoFT gene showed an early-flowering phenotype. Conversely, in roses, RoFT was continuously expressed after floral bud formation, and RoFT transcript accumulation reached its peak after that of the floral meristem identity gene RoAP1b. These data suggest that RoFT may be essential not only for floral transition but also for normal floral development and flowering in roses

RNA-mediated epigenetic modifications of an endogenous gene targeted by a viral vector—a potent gene silencing system to produce a plant that does not carry a transgene but has altered traits

Nucleotide-sequence-specific interactions mediated by double-stranded RNA (dsRNA) can induce gene silencing. Gene silencing through transcriptional repression can be induced by dsRNA targeted to a gene promoter. However, until recently, no plant has been produced that harbors an endogenous gene that remains silenced in the absence of promoter-targeting dsRNA. We have reported for the first time that transcriptional gene silencing can be induced by targeting dsRNA to the endogenous gene promoters in petunia and tomato plants, using a Cucumber mosaic virus (CMV)-based vector and that the induced gene silencing is heritable. Efficient silencing depended on the function of the 2b protein encoded in the vector, which facilitates epigenetic modifications through the transport of short interfering RNA (siRNA) to the nucleus. Here we show that gene silencing that is mediated by targeting dsRNA to a gene promoter via the CMV vector can be as strong as co-suppression in terms of both the extent of mRNA decrease and phenotypic changes. We also show that the expression of genes involved in RNA-directed DNA methylation and in demethylation are upregulated and downregulated, respectively, in Arabidopsis plants infected with CMV. Thus, along with the function of the 2b protein, that transports siRNA to the nucleus, the promoter-targeted silencing system using the CMV vector has some property that facilitates heritable epigenetic changes on endogenous genes, enabling the production of a novel class of modified plants that do not have a transgene